Search results for "Retinal Degeneration"

showing 10 items of 59 documents

Mutation ofPOC1Bin a Severe Syndromic Retinal Ciliopathy

2014

We describe a consanguineous Iraqi family with Leber congenital amaurosis (LCA), Joubert syndrome (JBTS), and polycystic kidney disease (PKD). Targeted next-generation sequencing for excluding mutations in known LCA and JBTS genes, homozygosity mapping, and whole-exome sequencing identified a homozygous missense variant, c.317G>C (p.Arg106Pro), in POC1B, a gene essential for ciliogenesis, basal body, and centrosome integrity. In silico modeling suggested a requirement of p.Arg106 for the formation of the third WD40 repeat and a protein interaction interface. In human and mouse retina, POC1B localized to the basal body and centriole adjacent to the connecting cilium of photoreceptors and in …

MaleRetinal degenerationgenetic structuresAmino Acid MotifsLeber Congenital AmaurosisMolecular Sequence DataCell Cycle ProteinsBiologyKidneyArticleRetinaJoubert syndromeMiceCerebellar DiseasesCerebellumCiliogenesisRetinitis pigmentosaGeneticsmedicineAnimalsHumansAbnormalities MultipleAmino Acid SequenceCiliaEye AbnormalitiesChildZebrafishGenetics (clinical)Cystic kidneyGeneticsCiliumKidney Diseases Cysticmedicine.diseaseDisease gene identificationeye diseasesPedigreeCiliopathyGene Knockdown TechniquesIraqMutationsense organsHuman Mutation
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Intravitreal Docosahexaenoic Acid in a Rabbit Model: Preclinical Safety Assessment

2014

PurposeThe purpose of the present study was to evaluate the retinal toxicity of a single dose of intravitreal docosahexaenoic acid (DHA) in rabbit eyes over a short-term period.MethodsSixteen New Zealand albino rabbits were selected for this pre-clinical study. Six concentrations of DHA (Brudy Laboratories, Barcelona, Spain) were prepared: 10 mg/50 µl, 5 mg/50 µl, 2'5 mg/50 µl, 50 µg/50 µl, 25 µg/50 µl, and 5 µg/50 µl. Each concentration was injected intravitreally in the right eye of two rabbits. As a control, the vehicle solution was injected in one eye of four animals. Retinal safety was studied by slit-lamp examination, and electroretinography. All the rabbits were euthanized one week a…

MaleRetinal degenerationgenetic structuresÀcids grassosPharmacologyBiochemistryMicechemistry.chemical_compoundCorneaMedicine and Health SciencesRatolinsExperimentació animalDegeneració (Patologia)Multidisciplinarymedicine.diagnostic_testQFatty AcidsChromatographic TechniquesRDegeneration (Pathology)Animal ModelsLipidsChemistrymedicine.anatomical_structureNeurologyDocosahexaenoic acidPhysical SciencesMedicineRetinal DisordersRabbitsSafetyAnatomyResearch Articlemedicine.medical_specialtyHistologyDrug Research and DevelopmentDocosahexaenoic AcidsNew Zealand AlbinoScienceOcular AnatomyResearch and Analysis MethodsRetinaInjectionsAqueous HumorModel OrganismsOcular SystemElectroretinographyToxicity Tests AcutemedicineAnimalsFatty acidsGas ChromatographyPharmacologyDose-Response Relationship Drugbusiness.industrySignificant differenceBiology and Life SciencesRetinalmedicine.diseaseSurgeryVitreous BodyOphthalmologychemistryNeuro-OphthalmologyAnimal experimentationRabbit modelClinical MedicinebusinessElectroretinographyPLoS ONE
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Electroretinographic response in WAG/Rij rats after low-intensity cyclic light exposure.

1993

In order to investigate the combined influence of age and light, the b-wave and oscillatory potentials (OPs) of the electroretinogram (ERG) were recorded in 1.5-, 7- and 12-month-old WAG/Rij rats, reared under homogenous low-intensity cyclic light exposure. Wistar albino rats of the same ages, reared under the same conditions, served as controls. The b-wave amplitude decreased, and its implicit time increased in the older age groups significantly more in WAG/Rij than in Wistar rats. Statistical analysis indicated that the b-wave amplitude is a more suitable parameter than implicit time in differentiating the ERG variations of one rat strain from the other. The added amplitude of the OPs als…

Malemedicine.medical_specialtyAgingPeriodicitygenetic structuresOscillatory potentialsLightDark AdaptationRetinaCellular and Molecular NeuroscienceOpticsAge groupsInternal medicinemedicineElectroretinographyAnimalsStatistical analysisRats WistarLight exposuremedicine.diagnostic_testChemistrybusiness.industryRetinal DegenerationRat strainRats Inbred StrainsGeneral MedicineSensory SystemsIntensity (physics)RatsOphthalmologyEndocrinologyFemalebusinessErgElectroretinographyOphthalmic research
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Demonstration of retinal afferents in the RCS rat, with reference to the retinohypothalamic projection and suprachiasmatic nucleus.

1995

In the Royal College of Surgeons (RCS) rat, characterized by inherited retinal dystrophy, retinal projections to the brain were studied using anterograde neuronal transport of cholera toxin B subunit upon injection into one eye. The respective immunoreactivity was found predominantly contralateral to the injection site in the lateral geniculate nucleus, superior colliculus, nucleus of the optic tract, medial terminal nucleus of the accessory optic tract, and bilateral hypothalamic suprachiasmatic nuclei. Although terminal density was somewhat reduced in dystrophic rats, the projection patterns in these animals appeared similar to those seen in their congenic controls and were comparable to …

Malemedicine.medical_specialtyCholera ToxinHistologyOptic tractHypothalamusBiologyLateral geniculate nucleusRetinaPathology and Forensic MedicineInternal medicinemedicineAnimalsNeuropeptide YNeuronal transportRetinaAfferent PathwaysSuprachiasmatic nucleusSuperior colliculusRetinal DegenerationGeniculate BodiesRats Inbred StrainsCell BiologyRatsEndocrinologymedicine.anatomical_structureHypothalamusFemaleSuprachiasmatic NucleusRetinohypothalamic tractVasoactive Intestinal PeptideCell and tissue research
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Norrie gene product is necessary for regression of hyaloid vessels.

2004

To investigate the nature and origin of the vitreous membranes in mice with knock-out of the Norrie gene product (ND mice).Eighty-two eyes of ND mice of different age groups (postnatal day [P]0-13 months) and 95 age-matched wild-type control mice were investigated. In vitreoretinal wholemounts and in sagittal sections, vessels and free cells were visualized by labeling for lectin. In addition, staining with a marker for macrophages (F4/80) and collagen XVIII/endostatin known to be involved in regression of hyaloid vessels was performed for light and electron microscopic investigations. Endostatin expression was confirmed by Western blot analysis.Wild-type controls showed the typical pattern…

Pathologymedicine.medical_specialtygenetic structuresAngiogenesisBlotting WesternNerve Tissue ProteinsBiologyRetinal NeovascularizationBlindnessGene productchemistry.chemical_compoundMiceVasculogenesismedicineAnimalsEye AbnormalitiesEye ProteinsMicroscopy ImmunoelectronMice KnockoutMembranesRetinal DegenerationRetinal VesselsRetinalGenetic Diseases X-LinkedAnatomyAntigens Differentiationeye diseasesEndostatinsVitreous Bodymedicine.anatomical_structurechemistryCirculatory systemcardiovascular systemsense organsEndostatinBlood vesselInvestigative ophthalmologyvisual science
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AAV-Mediated Clarin-1 Expression in the Mouse Retina: Implications for USH3A Gene Therapy

2015

Usher syndrome type III (USH3A) is an autosomal recessive disorder caused by mutations in clarin-1 (CLRN1) gene, leading to progressive retinal degeneration and sensorineural deafness. Efforts to develop therapies for preventing photoreceptor cell loss are hampered by the lack of a retinal phenotype in the existing USH3 mouse models and by conflicting reports regarding the endogenous retinal localization of clarin-1, a transmembrane protein of unknown function. In this study, we used an AAV-based approach to express CLRN1 in the mouse retina in order to determine the pattern of its subcellular localization in different cell types. We found that all major classes of retinal cells express AAV…

Photoreceptors0301 basic medicineRetinal degenerationSensory ReceptorsPhysiologyUsher syndromeCell Membraneslcsh:MedicineSocial SciencesNervous SystemPhotoreceptor cellMicechemistry.chemical_compound0302 clinical medicineAnimal CellsMedicine and Health SciencesPsychologylcsh:ScienceNeuronsRegulation of gene expressionGeneticsMultidisciplinaryRetinal DegenerationAnimal ModelsDependovirusCell biologyElectrophysiologymedicine.anatomical_structureSensory PerceptionCellular TypesAnatomyCellular Structures and OrganellesUsher SyndromesResearch ArticleSignal TransductionCell typeImaging TechniquesOcular AnatomyNeurophysiologyOuter plexiform layerMouse ModelsBiologyResearch and Analysis MethodsRetina03 medical and health sciencesModel OrganismsOcular SystemFluorescence ImagingmedicineAnimalsHumansRetinalcsh:RMembrane ProteinsBiology and Life SciencesAfferent NeuronsRetinalGenetic TherapyCell Biologymedicine.diseaseDisease Models Animal030104 developmental biologyGene Expression RegulationchemistrySynapsesEyeslcsh:QHead030217 neurology & neurosurgeryNeurosciencePLOS ONE
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Polyglutamine toxicity induces rod photoreceptor division, morphological transformation or death in Spinocerebellar ataxia 7 mouse retina

2010

In neurodegenerative disorders caused by polyglutamine (polyQ) expansion, polyQ toxicity is thought to trigger a linear cascade of successive degenerative events leading to neuronal death. To understand how neurons cope with polyQ toxicity, we studied a Spinocerebellar ataxia 7 (SCA7) mouse which expresses polyQ-expanded ATXN7 only in rod photoreceptors. We show that in response to polyQ toxicity, SCA7 rods go through a range of radically different cell fates, including apoptotic and non-apoptotic cell death, cell migration, morphological transformation into a round cell or, most remarkably, cell division. The temporal profile of retinal remodeling indicates that some degenerative pathways …

Programmed cell deathCell divisionProliferationPopulationMice TransgenicNerve Tissue ProteinsBiologylcsh:RC321-571Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell MovementRetinal Rod Photoreceptor CellsmedicineAnimalsSpinocerebellar AtaxiasNeurodegenerationeducationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCell ShapeComputingMilieux_MISCELLANEOUSSpinocerebellar ataxia 7030304 developmental biologyAtaxin-7Mice Knockout0303 health sciencesRetinaeducation.field_of_studyPhotoreceptorCell DeathRetinal DegenerationNeurodegenerationRetinalmedicine.diseaseRemodelingMice Inbred C57BLmedicine.anatomical_structureNeurologyProteotoxicitychemistryNerve DegenerationSpinocerebellar ataxia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Apoptosis Regulatory ProteinsPeptidesPolyglutamineNeuroscience030217 neurology & neurosurgery
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Genetic variants linked to myopic macular degeneration in persons with high myopia: CREAM Consortium.

2019

Purpose: To evaluate the roles of known myopia-associated genetic variants for development of myopic macular degeneration (MMD) in individuals with high myopia (HM), using case-control studies from the Consortium of Refractive Error and Myopia (CREAM). Methods: A candidate gene approach tested 50 myopia-associated loci for association with HM and MMD, using meta-analyses of case-control studies comprising subjects of European and Asian ancestry aged 30 to 80 years from 10 studies. Fifty loci with the strongest associations with myopia were chosen from a previous published GWAS study. Highly myopic (spherical equivalent [SE] ≤ -5.0 diopters [D]) cases with MMD (N = 348), and two sets of cont…

Refractive errorCandidate genegenetic structuresEmmetropiaGenome-wide association studySensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Macular DegenerationMathematical and Statistical TechniquesMedicine and Health SciencesMyopiaGeriatric OphthalmologyDioptreVisual ImpairmentsAged 80 and overMultidisciplinaryQRetinal DegenerationStatisticsRGenomicsMetaanalysisPhenotypeResearch DesignPhysical SciencesMedicineRetinal DisordersFemaleAnatomyResearch Articlemedicine.medical_specialtyScienceOcular AnatomySingle-nucleotide polymorphismResearch and Analysis MethodsRetinaOcular SystemOphthalmologyGeneticsGenome-Wide Association StudiesmedicineHumansStatistical Methodsbusiness.industryGene Expression ProfilingCase-control studyBiology and Life SciencesComputational BiologyGenetic VariationCorrectionHuman GeneticsMacular degenerationGenome Analysismedicine.diseaseeye diseasesOphthalmologyGenetic LociGeriatricsMacular DisordersCase-Control StudiesEyessense organsbusinessHeadMathematicsPloS one
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Preclinical Retinal Neurodegeneration in a Model of Multiple Sclerosis

2012

Neurodegeneration plays a major role in multiple sclerosis (MS), in which it is thought to be the main determinant of permanent disability. However, the relationship between the immune response and the onset of neurodegeneration is still a matter of debate. Moreover, recent findings in MS patients raised the question of whether primary neurodegenerative changes can occur in the retina independent of optic nerve inflammation. Using a rat model of MS that frequently leads to optic neuritis, we have investigated the interconnection between neurodegenerative and inflammatory changes in the retina and the optic nerves with special focus on preclinical disease stages. We report that, before manif…

Retinal Ganglion CellsPathologyTime FactorsStilbamidinesgenetic structuresJournal ClubFreund's Adjuvantchemistry.chemical_compoundBlood-Retinal BarrierStudent’s SectionCell DeathMicrogliabiologyGeneral NeuroscienceRetinal DegenerationNeurodegenerationArticlesmedicine.anatomical_structureSpinal CordRetinal ganglion cellOptic nerveFemaleMicrogliaMyelin Proteinsmedicine.medical_specialtyMultiple SclerosisEnzyme-Linked Immunosorbent AssayRetinaMyelin oligodendrocyte glycoproteinMicroscopy Electron TransmissionAntigens CDOccludinGlial Fibrillary Acidic ProteinIn Situ Nick-End LabelingmedicineAnimalsOptic neuritisAquaporin 4Retinabusiness.industryMacrophagesMultiple sclerosisMembrane ProteinsRetinalOptic Nervemedicine.diseaseeye diseasesRatsDisease Models Animalchemistrybiology.proteinMyelin-Oligodendrocyte Glycoproteinsense organsbusinessNeuroscienceThe Journal of Neuroscience
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Retinal microglia are activated by systemic fungal infection

2014

Purpose: To determine whether systemic fungal infection could cause activation of retinal microglia and therefore could be potentially harmful for patients with retinal degenerative diseases. Methods: Activation of retinal microglia was measured in a model of sublethal invasive candidiasis in C57BL/6J mice by (i) confocal immunofluorescence and (ii) flow cytometry analysis, using anti-CD11b, anti-Iba1, anti-MHCII and anti-CD45 antibodies. Results: Systemic fungal infection causes activation of retinal microglia, with phenotypic changes in morphology, surface markers expression, and microglial re-location in retinal layers. Conclusions: As an excessive or prolonged microglial activation may …

Retinal Ganglion CellsSystemic mycosisFarmacologíaBiología CelularAxonal TransportRetinachemistry.chemical_compoundMicemedicineAnimalsMicroglial activationInflammationMicroscopy ConfocalMicrogliabusiness.industryRetinal DegenerationCandidiasisRetinalFlow CytometryImmunohistochemistryMice Inbred C57BLDisease Models Animalmedicine.anatomical_structurechemistryImmunologyChristian ministryFemaleMicrogliabusinessInfection
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